However, the precise mechanisms whereby oncogenic signalling emanating from RTKs promotes the invasive phenotype of GBM cells are largely unknown, although some mediators have been proposed to play an important role, such as Rac guanine-nucleotide exchange factor (GEF) Dock180 that has been shown to be activated downstream of EGFR, PDGFR and c-Met [35,36,37]. The gene discussed is MET; the disease is glioblastoma.